ArticleThe Journal of biological chemistry2009
Cytolethal distending toxin-induced cell cycle arrest of lymphocytes is dependent upon recognition and binding to cholesterol.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 78 citations in OpenAlex.
- Review
- Wild raccoons (Microbiology spectrum · 2025Article
- Article
- Cellugyrin (synaptogyrin-2) dependent pathways are used by bacterial cytolethal distending toxin and SARS-CoV-2 virus to gain cell entry.Frontiers in cellular and infection microbiology · 2024Article
- Delivery, structure, and function of bacterial genotoxins.Virulence · 2022Review
- Article
- The Active Subunit of the Cytolethal Distending Toxin, CdtB, Derived From BothFrontiers in cellular and infection microbiology · 2021Article
- From DNA Damage to Cancer Progression: Potential Effects of Cytolethal Distending Toxin.Frontiers in immunology · 2021Review
- Cytolethal distending toxin-induced release of interleukin-1β by human macrophages is dependent upon activation of glycogen synthase kinase 3β, spleen tyrosine kinase (Syk) and the noncanonical inflammasome.Cellular microbiology · 2020Article
- Herpesvirus-bacteria synergistic interaction in periodontitis.Periodontology 2000 · 2020Review
- The Cell-Cycle Regulatory Protein p21Pathogens (Basel, Switzerland) · 2020Article
- Internalization and Intoxication of Human Macrophages by the Active Subunit of theFrontiers in immunology · 2020Article
- Genome-Wide Identification of Host Genes Required for Toxicity of Bacterial Cytolethal Distending Toxin in a Yeast Model.Frontiers in microbiology · 2019Article
- Catechin-mediated restructuring of a bacterial toxin inhibits activity.Biochimica et biophysica acta. General subjects · 2019Article
- Article
- Impact of Dietary Cholesterol on the Pathophysiology of Infectious and Autoimmune Disease.Nutrients · 2018Review
- Internalization of the Active Subunit of theFrontiers in cellular and infection microbiology · 2017Article
- Use of a Cholesterol Recognition Amino Acid Consensus Peptide To Inhibit Binding of a Bacterial Toxin to Cholesterol.Biochemistry · 2016Article
- Inhibition of Bacterial Toxin Activity by the Nuclear Stain, DRAQ5™.The Journal of membrane biology · 2016Article
- Inhibition of LtxA toxicity by blocking cholesterol binding with peptides.Molecular oral microbiology · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Induction of cell cycle arrest in lymphocytes after exposure to the Aggregatibacter actinomycetemcomitans cytolethal distending toxin (Cdt) is dependent upon the integrity of lipid membrane microdomains. In this study we further demonstrate that the association of Cdt with lymphocyte plasma membranes is dependent upon binding to cholesterol. Depletion of cholesterol resulted in reduced toxin binding, whereas repletion of cholesterol-depleted cells restored binding. We employed fluorescence resonance energy transfer and surface plasmon resonance to demonstrate that toxin association with model membranes is dependent upon the concentration of cholesterol; moreover, these interactions were cholesterol-specific as the toxin failed to interact with model membranes containing stigmasterol, ergosterol, or lanosterol. Further analysis of the toxin indicated that the CdtC subunit contains a cholesterol recognition/interaction amino acid consensus (CRAC) region. Mutation of the CRAC site resulted in decreased binding of the holotoxin to cholesterol-containing model membranes as well as to the surface of Jurkat cells. The mutant toxin also exhibited reduced capacity for intracellular transfer of the active toxin subunit, CdtB, as well as reduced toxicity. Collectively, these observations indicate that membrane cholesterol serves as an essential ligand for Cdt and that this association can be blocked by either depleting membranes of cholesterol or mutation of the CRAC site.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.